I’ll be talking on Wisconsin Public Radio with host Ben Merens about ebooks and the future of publishing. I’ll be on for the hour from 5 pm to 6 pm CT (6-7 ET) You can listen live here.

Michael Osterholm, his face a pink-cheeked scowl, looked out across the table, beyond the packed room at the New York Academy of Sciences, and out through the windows. The New York Academy of Sciences is housed on the fortieth floor of 7 World Trade Center, and their endless bank of windows affords a staggering view of Manhattan, Brooklyn, and New Jersey. One reason that its view is so magnificent is that there’s a huge gap in the skyline–and a huge gouge in the ground–where the Twin Towers once stood.

Osterholm had come here from Minnesota, where he runs a research center for infections diseases and terrorism, to talk Thursday night about the threat of a new kind of flu sitting in labs in the Netherlands and Wisconsin. In nature, it’s a flu that spreads easily between birds but doesn’t travel well from human to human. The Dutch and Wisconsin scientists had found ways to get this bird flu, known as H5N1, to move between ferrets. For Osterholm, ferrets were uncomfortably close to humans on the evolutionary tree. And so he, along with other members of an advisory board, issued a recommendation in December that key information in the papers about the research should be left out.

Osterholm looked out at the empty space beyond the windows. “Who would have imagined that you could use box cutters to take down the World Trade Center?” Osterholm asked. The risk from the new bird flu might seem equally unlikely, he warned, but it could end up being far more devastating. “We can’t afford to be wrong.”

The bird flu controversy first started to bubble up in September, when Ron Fouchier of the Erasmus Medical Center in Rotterdam described some of his unpublished results at a scientific meeting in Malta. It kicked into high gear when the National Science Advisory Board on Biosecurity issued their ruling, which Fouchier and Yoshihiro Kawaoka have agreed to. In January, the researchers agreed to stop doing any H5N1 research for two months, during which time the scientific community would try to come up with a plan about how to deal with such controversial research.

Viruses very often spark controversies, but often the controversy is between the scientists who study them and groups of people beyond the academy. Think of HIV denialism, of the non-existent link between vaccines and autism, of the purported connection between the XMRV virus and chronic fatigue syndrome. The new bird flu controversy is different. It’s split the scientific community wide open. I’ve written about this controversy in recent weeks over at Slate, as well as here at the Loom. Like most reporters covering the story, I’ve sampled the sharply opposing viewpoints of scientists over the phone or via emails. But on Thursday night, we got to see this debate in person. The New York Academy of Sciences brought together a group of experts to talk about new virus, and whether self-censorship is a prudent protection or a dangerous precedent. I wasn’t sure what to expect; I was a bit worried it might have turned out to be a fairly dry discussion of how to inspect the hood equipment in virus labs. Instead, we witnessed explosive confrontation between scientists who think we may be facing a world-destroying catastrophe, and others who think our fear of non-existent threats is going to destroy science’s power to help us out of clear and present dangers.

The panel included two members of the National Science Advisory Board on Biosecurity: Michael Osterholm and Arturo Casadevall of Albert Einstein College of Medicine. They both made it clear that they were speaking at the meeting as individuals, rather than as official spokesmen for the board. But they presented a fairly united front. The board has been around for eight years, and it has only considered issuing a recommendation twice. The first time was in 2005, when scientists unearthed the bodies of victims of the 1918 flu epidemic, which killed an estimated 50 million people. The researchers isolated the 1918 virus and sequenced its genes. The board decided they had no objections about publishing the research. But six years later, they decided that, as bad as the 1918 flu might have been, the risk of an H5N1 outbreak was worse.

One big factor in their recent decision was the mortality rate when H5N1 gets into people. The World Health Organization’s official estimate is 60%. The 1918 flu, by contrast, had a death rate of about two percent. If H5N1 could gain the ability to spread among humans–either naturally, or through a lab experiment–it could bring that fearsome death rate to the entire world. “It’s the lion king of infectious diseases,” Osterholm said, no doubt dismaying Disney lawyers across the country.

Sitting a few seats down the panel from Osterholm was Peter Palese, one of the world’s leading experts on flu, who works at Mount Sinai Medical School. Palese disputed Osterholm’s apocalyptic warnings. Where Osterholm burned hot, Palese kept cool, but he did not hide his utter rejection of the board’s decision. Just because a flu virus can be transmitted by another mammal species, he argued, doesn’t automatically mean it can spread among humans. In fact, ferrets are rather delicate in the face of a flu infections, easily suffering from brain damage. Our closer relatives among the primates, by contrast, don’t get sick from flu at all. (Jon Cohen explores the ferret question in depth in a news article for Science.)

Palese also questioned whether H5N1 is all that dangerous. He argued that the World Health Organization based its mortality rate only on the people who came into hospitals and tested positive for H5N1. But this particular strain of bird flu mostly strikes people in poor countries, especially in southeast Asia, where medical services are scarce. The people who make it to a hospital could well be a small fraction of all the people who come down with H5N1.

“The asymptomatic people are not being counted,” Palese said. If those extra people only got sick for a few days and then got on with their lives, the true mortality rate might be far less than 60% “It’s really much lower,” he said, pointing to surveys in Thailand and other countries that revealed evidence that a fair number of people had been exposed to H5N1 at some point in the past. (Palese recently published this same argument in the Proceedings of the National Academy of Sciences.)

This argument positively enraged Osterholm. He had clearly read Palese’s recent PNAS commentary and had prepared a rebuttal. “What you’re saying is just propaganda,” he told Palese. The trouble with Palese’s numbers were that they came from lousy studies, Osterholm argued. There are many ways to overestimate how many people have been exposed to a particular virus. A common test involves fishing for antibodies in blood samples. If your test isn’t precise enough, you may end up dredging up antibodies to other viruses. Osterholm had gone through surveys of H5N1 exposure, setting aside the lousy studies and tallying up the results from the best of the bunch. He came up with an estimate of .6% or less. If very few people have been exposed, the recorded deaths from H5N1 represent a frighteningly high rate.

Casadevall granted that perhaps H5N1 wasn’t 60% fatal. But it could be half that and still be a planetary nightmare. Even if it was ten times lower, it would still be far worse than the 1918 flu. “The numbers of unbelievable, any way you look at it,” he said.

Palese was unmoved. The new H5N1 viruses might pose a risk–a small one, in Palese’s mind–but scientists could handle it. All the research that had triggered the controversy wasn’t conducted in someone’s backyard. It was carried out in well-protected labs. Palese noted that the board doesn’t seem to have any objections to the work that’s done these days on smallpox, a virus that killed millions of people every year until it was eradicated in the 1970s. If scientists can in fact safely experiment with dangerous viruses, there is no need to paralyze the scientific community over bird flu. “You can always assume the worst,” Palese said. “But where do we stop being afraid?”

Osterholm glowered at Palese. “You do not represent the mainstream of influenzologists when it comes to this issue on influenza,” he said. I glanced at some of the other journalist in the audience, wondering if Osterholm could see us scribbling notes.

Osterholm stressed that he was not against research on bird flu in general. He just wanted the scientific community to balance the potential costs and benefits. He didn’t see very much significance in the new bird flu work. It wouldn’t help public health workers monitoring H5N1 viruses for lineages that might be evolving into a human pathogen. Nor did he see any benefit for developing vaccines or antivirals. On the other hand, he saw a risk–a small one, possibly–of tremendous devastation.

But when it comes to viruses can we really calculate such ratios of costs to benefits? Vincent Racaniello, a Columbia University virologist who was also on the panel, doesn’t think so. We’re bad at estimating risks. In 1981, for example, Racaniello and his colleagues pioneered a method for making polio viruses: they stuck the virus’s genes on a ring of DNA called a plasmid, which they then inserted into E. coli bacteria. The engineered E. coli spewed out polio genes, which Racaniello could insert into human culture cells, which then made full-blown polio viruses. People worried that Racaniello’s bacteria would get into people’s guts and start a polio epidemic. (It didn’t.)

We’re also bad at determining the benefits of research. Racaniello recalled how microbiologists in the 1950s discovered that E. coli defend themselves against invading viruses by chopping up their genes. Nobody thought much of that discovery for over a decade. But then in the late 1960s, a few researchers realized that they could use E. coli’s enzymes to cut up DNA and then paste them into new combinations. The entire biotechnology industry was born from that late eureka.

“You could have never predicted that,” said Racaniello. “You never know who will do the right experiment. So that’s why you need to give the information to everyone.”

The way things stand right now, everyone will not be getting that information. I tried to follow the reasoning for holding back key parts of the studies, but, honestly, I can’t recount it in a way that makes sense. As far as I could tell, the thinking was somebody just fooling around out of curiosity would be able to use the full information to create a deadly flu. But the fact is that the scientists who produced the new bird flu used standard methods that have been published many times over. I was also confused by how Nature and Science, the two journals where the redacted papers are to be published, will handle distributing the information to those who need to know about it. An editor from Nature talked about how hard it would be to set up a system. I had been expecting them to have a system to unveil for us.

“None of us ever wants to see a redaction again,” said Casadevall. The most sensible way to avoid that would be to figure out a way to make decisions about risks and benefits much earlier in the life cycle of an experiment. If the mission of an experiment is to create a deadly virus, just to see if it can be done, the panelists agreed that that is probably not a study to run. But what kind of system can stop not just these experiments, but other experiments that might present unexpected dangers? Casadevall worries that every graduate student may have to fill out 100-page forms for even the most harmless of experiments. “You’ll kill science,” he said.

Casadevall was expressing a concern that all the scientists on the panel shared: they worry that this affair will keep them from doing research. For now, they’re trying to work out a fairly self-regulating system to handle this sort of controversial research, perhaps in the hopes that the government won’t come sweeping in. But there was one non-scientist on the panel who did her best to make the scientists aware of the world outside their community.

Laurie Garrett, an award-winning health reporter who now works at the Council on Foreign Relations, pointed out that the flu is not just something that American scientists study in their labs. It’s a global problem. There’s a huge amount of resentment in poor countries where bird flu is the biggest threat, not just to humans, but to the poultry industry. “Poor people are killing their chickens for you,” Garrett said. “They’re going bankrupt.”

Making matters worse, as Garrett has recently written, is the distrust that has developed in the developing world towards Western medical research and the pharmaceutical industry. Indonesia, where many of the H5N1 deaths have occurred, has been reluctant to share bird flu samples with Western scientists, for fear that they would make huge profits from vaccines developed from them. The World Health Organization has set up an international agreement for the exchange of wild bird flu strains between different countries, but it’s in fragile shape.

So for all the sparks that flew in New York Thursday night, the real fireworks over the flu are yet to come.

[Update 2/3 9 am: Corrected description of Racaniello's experiment. Thanks to Matt Frieman. 2:50 pm Fixed Fouchier's institution name and month of his talk. Thanks to Jon Cohen. 8 pm: Expanded Osterholm's "mainstream of influenzologists" quote after seeing his objection to a similarly truncated version in Christine Gorman's story for Scientific American and reviewing my own recording. It's a valid clarification .]

The novelist Jonathan Franzen delivered quite a rant about e-books the other day. He’s deeply wrong, as I explain at the Crux by going shopping for a copy of The Great Gatsby. Check it out.

Thousands of papers get published every week, but every now and then a truly strange one pops up. On December 23, a new journal called Life published a paper by Case Western Reserve University biochemist Eric Andrulis called “Theory of the Origin, Evolution, and Nature of Life.”

At Ars Technica, John Timmer unpacks this 105-page paper and delves into the weirdness, in a post called “How the craziest f#@!ing paper got published and promoted.”

The basic idea is that everything, from subatomic particles to living systems, is based on helical systems the author calls “gyres,” which transform matter, energy, and information. These transformations then determine the properties of various natural systems, living and otherwise. What are these gyres? It’s really hard to say; even Andrulis admits that they’re just “a straightforward and non-mathematical core model” (although he seems to think that’s a good thing). Just about everything can be derived from this core model; the author cites “major phenomena including, but not limited to, quantum gravity, phase transitions of water, why living systems are predominantly CHNOPS (carbon, hydrogen, nitrogen, oxygen, phosphorus, and sulfur), homochirality of sugars and amino acids, homeoviscous adaptation, triplet code, and DNA mutations.”

He’s serious about the “not limited to” part; one of the sections describes how gyres could cause the Moon to form.

Is this a viable theory of everything? The word “boson,” the particle that carries forces, isn’t in the text at all. “Quark” appears once—in the title of one of the 800 references. The only subatomic particle Andrulis describes is the electron; he skips from there straight up to oxygen. Enormous gaps exist everywhere one looks.

The theory is supposed to be testable, but the word “test” only shows up in the text twice. In both cases, Andrulis simply claims his theory is testable in specific areas of study. He does not indicate what those tests might be, nor what results would be predicted based on his gyres.

I could easily go into more specifics (very easily—I’ve got lots of notes), but it’s clear that there’s nothing in the paper that much resembles science.

Timmer goes on to look at how the paper glided smoothly into the science media machine, first with a press release from Case Western , and then with reprints of said press release at outlets like Science Daily and Physorg, without anyone wondering if it deserved this sort of attention.

I wondered how the paper got published and checked out the editorial board of Life. One name popped out at me: Stephen Mojzsis, a University of Colorado geochemist. I met Mojzsis while working on a story about the age of the Earth for National Geographic, and I’ve stayed in touch on and off ever since.  I dropped him a note Sunday to ask about the paper. To which he replied,

“You saw it before me!  I am pretty unhappy about it.  Have just contacted the Editor in Chief.”

The more Mojzsis looked into it, the less he liked the situation. Yesterday he tendered his resignation from the board. Today his name is gone from the journal’s web site, along with a number of other editors.

I have to scramble today to get ready for a talk at the University of Maryland tomorrow, so I won’t be digging deep into this story. I’d suggest you keep up with Timmer, as well as Ivan Oransky at Retraction Watch, to see how this drama unfolds.

Charles Darwin recognized that natural selection can make eyes sharper, muscles stronger, and fur thicker. But evolution does more than just improve what’s already there. It also gives rise to entirely new things—like eyes and muscles and fur. To study how new things evolve, biologists usually have to rely on ancient clues left behind for hundreds of millions of years. But in a study published today, scientists at Michigan State University show that it’s possible to watch something new evolve in front of their eyes, in just a couple weeks.

The scientists were studying a virus, which evolved a new way of invading cells. As a result, their research not only sheds light on a fundamental question about evolution. It also suggests that it may worryingly easy for viruses such as influenza to turn into new epidemics. Check it out.

[Image of lambda virus: AJC1 on Flickr via Creative Commons]

A fair number of scientists like to get a tattoo to celebrate their research. Ryan Carney, a biologist at Brown University has taken the practice one step further. He’s gotten a tattoo that shows the key finding of a paper he and his colleagues have just published today. They studied a fossil feather from Archaeopteryx, the iconic bird (or almost-bird). They conclude it looked just like this tattoo.

Carney collaborated on the research with a team of scientists who have developed a method to reconstruct colors from fossils. One source of colors in animals is a cellular structure called a melanosome. Depending on the size, shape, and spacing of melanosomes, they can produce a range of hues. It turns out that melanosomes are incredibly rugged, sometimes enduring for millions of years.

As I wrote in the New York Times in 2009, the scientists first found melanosomes in the ink sac of a fossil squid and then went on to look at a 47-million-year-old bird feather.  Then they went on to look at the feathers and feather-like structures of dinosaurs, reconstructing some of the colors of their plumage. The color pattern, which included stripes and tufts, hints that dinosaurs may have been using their feathers to show off to each other long before they evolved flight. (More details can be found in this story I wrote for National Geographic last year.)

No examination of feather evolution would be complete, of course, without Archaeopteryx. For over 150 years, it’s been at the center of debates about the history of birds–not to mention evolution itself.

The first fossil of Archaeopteryx was a single feather–the one that Carney has turned into a tattoo. It was discovered in 1861 in a limestone quarry near the town of Solnhofen and brought to Hermann von Meyer, one of Germany’s leading paleontologists at the time. As scientists would later determine, this exceptional feather was 145 million years old. Despite its antiquity, the feather looked much like the feathers on the wings of living birds.

The fossil was so extraordinary that Von Meyer wondered if some forger had etched it. After all, Solnhofen limestone was prized for making finely detailed lithographic prints. But then von Meyer compared the slab and the counterslab and found them to be identical.

“No draughtsman could produce anything so real,” he declared.

Even as von Meyer was studying the feather, the quarry at Solhofen yielded another spectacular fossil: an entire animal cloaked in feathers. Word of the fossil spread fast, but only a few scientists got to glimpse the fossil in person. Its owner, a local doctor, was carefully managing the access to his fossil to fuel a bidding war for his entire fossil collection. Those few glimpses were enough to electrify scientists across Germany and beyond. The animal looked in some ways like a bird. It had wing feathers draped from its arms, for example. But other parts of its body looked more like a reptile’s, such as its long bony tail. It was unlike anything alive today.

At the end of 1861, Von Meyer came up with a name to describe both fossils: Archaeopteryx lithographica—the lithographic first bird.

The debut of Archaeopteryx 150 years ago was a case of beautiful timing. Just two years earlier, Charles Darwin had published The Origin of Species, in which he claimed that living animals had evolved from transitional ancestors. “Had the Solenhofen quarries been commissioned – by august command – to turn out a strange being a la Darwin – it could not have executed the behest more handsomely – than in the Archaeopteryx,” wrote the paleontologist Hugh Falconer.

Darwin agreed. “It is a grand case for me,” he confided to a friend.

In later years, more fossils of Archaeopteryx emerged, and it became even more of a chimera. Like a bird, it had feathers on its entire body. But unlike living birds, it had teeth in its mouth and claws on its wings. Darwin’s followers continued to argue that it marked a transition in the origin of birds. But opponents of Darwin and his followers argued that a single species—especially one with feathers no different than those on living birds—did not establish a full-blown transition.

“Their views must be at once rejected as fantastic dreams,” the German paleontologist Andreas Wagner declared.

Wagner turned out to be wrong. A number of bird-like dinosaurs have come to light in the years since the discovery of Archaeopteryx, and researchers have been able to work out many of their relationships to each other. There’s still plenty of debate about just how well Archaeopteryx itself could fly, as well as its precise place in the dinosaur-bird tree of life. Last July fellow Discover blogger Ed Yong wrote about a new study suggesting other dinosaurs were more closely related to living birds than Archaeopteryx.

In a study funded by the National Geographic Society, Carney and his colleagues were able to sample tiny bits of the original, lone Archaeopteryx fossil, housed in a museum in Germany. They examined its melanosomes, comparing them to the melanosomes in 115 living birds. As they report today, the feather was most likely straight black, as you see it in Carney’s tattoo.

While a single feather isn’t enough to reconstruct Archaeopteryx’s entire appearance, it does provide some interesting clues about the animal. The feather was what’s known as a covert, meaning that it was sandwiched in the middle of the wing, covering the primary flight feathers but covered in turn by the feathers at the wing’s leading edge. As a result, it was mostly hidden from sight. So its black color couldn’t have served to attract the opposite sex or to camouflage it from enemies. It’s possible that the whole wing was black, and this particular covert just went along on the evolutionary ride. It’s also possible, Carney and his colleagues speculate, that the melanosomes were serving another function in this particular feather. In living birds, melanosomes can block bacterial infections, and they can also make feathers hard, preventing them from breaking under the forces of flight.

As for the function of black pigmentation on the shoulders of biologists–well, that’s another story.

Reference: R.M. Carney et al, “New evidence on the colour and nature of the isolated Archaeopteryx feather.” Nature Communications 2012 doi: 10.1038/ncomms1642

This Tuesday I’ll be giving a talk at the New York Academy of Sciences about Science Ink–complete with live tattooed scientists!

Here are some of the details…

When: Tuesday, January 24, 2012, 7:00 PM – 8:30 PM. (A reception will follow.)
Where: The New York Academy of Sciences
7 World Trade Center
250 Greenwich Street, 40th floor
New York, NY 10007-2157
212.298.8600

Get $10 dollars off full-price tickets by using the promo code ZIMMER. Register here: http://www.nyas.org/scienceink

See you there!

In yesterday’s New York Times, I wrote about a new paper in which scientists report the evolution of single-celled yeast into multicellular snowflake-like “bodies.” Most (but not all) of the experts I contacted for the story had high praise for the study. (It also won an award when it was presented as a talk over the summer at the Society for the Study of Evolution.) Once the story appeared, however, some scientists took to Twitter to express their skepticism. As much as I like Twitter, this is one of the situations where it fails. You can’t have a conversation about genetics, lab strains versus wild types, etc., in 140 character chunks. At least not very satisfying ones.

So here’s what I decided to do last night. I used Storify to collect the comments of Leonid Kruglyak of Princeton and Michael Eisen of Berkeley, and then passed them on to Will Ratcliff, the lead author of the new study. He then responded. Below you’ll find the Storify tweets, and then Ratcliff’s response. Please continue the conversation in the comment thread. (And be sure to download the paper–it’s open access.)

Will Ratcliff responds:

Well, I don’t buy it that yeast are multicellular in nature. Certainly some yeast in nature form small clusters (like strain RM11), but as far as I know, these are the exception to the rule. Most strains isolated in nature are unicellular, or at most, flocculating (which I still count as unicellular but social). [CZ: "Flocculating" refers to the clumps that unrelated yeast cells form when they starve.]

Our yeast are not utilizing ‘latent’ multicellular genes and reverting back to their wild state. The initial evolution of snowflake yeast is the result of mutations that break the normal mitotic reproductive process, preventing daughter cells from being released as they normally would when division is complete. Again, we know from knockout libraries that this phenotype can be a consequence of many different mutations. This is a loss of function, not a gain of function. You could probably evolve a similar phenotype in nearly any microbe (other than bacteria, binary fission is a fundamentally different process). We find that it is actually much harder to go back to unicellularity once snowflake yeast have evolved, because there are many more ways to break something via mutation than fix it. The amazing thing we see is that we rapidly see adaptations to this adaptation. If we select for more rapid settling, snowflake yeast evolve to delay reproduction until the parent is larger, allowing it settle more quickly. We see the evolution of higher rates of apoptosis as a way to regulate the size and number of propagules produced. We show that the transition to multicellularity in yeast is surprisingly easy, and have no reason to suspect it would be any harder in other microbes with a reproductive process similar to yeast.

In the history of life, single-celled microbes have evolved into multicellular bodies at least 25 times. In our own lineage, our ancestors crossed over some 700 million years ago. In tomorrow’s New York Times, I write about a new study in which single-celled yeast evolved into multicellular forms–completely with juvenile and adult forms, different cell types, and the ability to split off propagules like plant cuttings. All this in a matter of weeks. Check it out.

(The paper is not yet online yet, but here’s the reference: “Experimental evolution of multicellularity,” William C. Ratcliff, R. Ford Denison, Mark Borrello, and Michael Travisano. Proceedings of the National Academy of Sciences. http://www.pnas.org/cgi/doi/10.1073/pnas.1115323109 )

Update: Here’s a Twitter-Storify-blog follow up on some reactions to the study.

Each year, literary agent and science salonista John Brockman poses a question about science and gets a slew of answers from scientists, writers, and other folks. This year’s question is

WHAT IS YOUR FAVORITE DEEP, ELEGANT, OR BEAUTIFUL EXPLANATION?

Brockman got 187 responses, totaling some 126,700 words. A book, you say! Well, if this year is like previous ones, this year’s answers will indeed become a book. But in the meantime, you can browse the answers for yourself, perhaps plucking out those of your favorite people. (Fellow Discover blogger cosmologist Sean Carroll chooses Einstein’s explanation of gravity, for example.)

I found this year’s question particularly thought-provoking. Why is it that we call an equation or a theory “beautiful”? They don’t have pretty hazel eyes. They aren’t desert landscapes. I’m not sure of the answer. Scientific explanations seem to be beautiful if they give sense to confusing complexity in a very short space. Or maybe we just like the feeling we get when we consider how our puny human brains can interpret the universe.

For a lot of physicists, the beauty of an equation seems to be a good hint that it’s probably true. But I’m always a bit suspicious of beauty as a guide to the natural world. A number of contributors selected Darwin’s theory of evolution as their favorite explanation, and there’s no doubt that’s both beautiful and true. But there have been some wonderfully beautiful accounts of the natural world that have proven awesomely wrong. I was reminded of this fact while working on a new version of my evolution textbook (this one’s for biology majors). I was re-researching how scientists first came to appreciate the vast age of our planet, and realized it was a bit more complicated than I had previously appreciated. So that’s what I chose as my answer, which I’m reprinting here in full:

A Hot Young Earth: Unquestionably Beautiful and Stunningly Wrong

Around 4.567 billion years ago, a giant cloud of dust collapsed in on itself. At the center of the cloud our Sun began to burn, while the outlying dust grains began to stick together as they orbited the new star. Within a million years, those clumps of dust had become protoplanets. Within about 50 million years, our own planet had already reached about half its current size. As more protoplanets crashed into Earth, it continued to grow. All told, it may have taken another fifty million years to reach its full size—a time during which a Mars-sized planet crashed into it, leaving behind a token of its visit: our Moon.

The formation of the Earth commands our greatest powers of imagination. It is primordially magnificent. But elegant is not the word I’d use to describe the explanation I just sketched out. Scientists did not derive it from first principles. There is no equivalent of E=mc2 that predicts how the complex violence of the early Solar System produced a watery planet that could support life.

In fact, the only reason that we now know so much about how the Earth formed is because geologists freed themselves from a seductively elegant explanation that was foisted on them 150 years ago. It was unquestionably beautiful, and stunningly wrong.

The explanation was the work of one of the greatest physicists of the nineteenth century, William Thompson (a k a Lord Kelvin). Kelvin’s accomplishments ranged from the concrete (figuring out how to lay a telegraph cable from Europe to America) to the abstract (the first and second laws of thermodynamics). Kelvin spent much of his career writing equations that could let him calculate how fast hot things got cold. Kelvin realized that he could use these equations to estimate how old the Earth is. “The mathematical theory on which these estimates are founded is very simple,” Kelvin declared when he unveiled it in 1862.

At the time, scientists generally agreed that the Earth had started out as a ball of molten rock and had been cooling ever since. Such a birth would explain why rocks are hot at the bottom of mine shafts: the surface of the Earth was the first part to cool, and ever since, the remaining heat inside the planet has been flowing out into space. Kelvin reasoned that over time, the planet should steadily grow cooler. He used his equations to calculate how long it should take for a molten sphere of rock to cool to Earth’s current temperature, with its observed rate of heat flow. His verdict was a brief 98 million years.

Geologists howled in protest. They didn’t know how old the Earth was, but they thought in billions of years, not millions. Charles Darwin—who was a geologist first and then a biologist later—estimated that it had taken 300 million years for a valley in England to erode into its current shape. The Earth itself, Darwin argued, was far older. And later, when Darwin published his theory of evolution, he took it for granted that the Earth was inconceivably old. That luxury of time provided room for evolution to work slowly and imperceptibly.

Kelvin didn’t care. His explanation was so elegant, so beautiful, so simple that it had to be right. It didn’t matter how much trouble it caused for other scientists who would ignore thermodynamics. In fact, Kelvin made even more trouble for geologists when he took another look at his equations. He decided his first estimate had been too generous. The Earth might be only 10 million years old.

It turned out that Kelvin was wrong, but not because his equations were ugly or inelegant. They were flawless. The problem lay in the model of the Earth to which Kelvins applied his equations.

The story of Kelvin’s refutation got a bit garbled in later years. Many people (myself included) have mistakenly claimed that his error stemmed from his ignorance of radioactivity. Radioactivity was only discovered in the early 1900s as physicists worked out quantum physics. The physicist Ernst Rutherford declared that the heat released as radioactive atom broke down inside the Earth kept it warmer than it would be otherwise. Thus a hot Earth did not have to be a young Earth.

It’s true that radioactivity does give off heat, but there isn’t enough inside the planet is to account for the heat flowing out of it. Instead, Kelvin’s real mistake was assuming that the Earth was just a solid ball of rock. In reality, the rock flows like syrup, its heat lifting it up towards the crust, where it cools and then sinks back into the depths once more. This stirring of the Earth is what causes earthquakes, drives old crust down into the depths of the planet, and creates fresh crust at ocean ridges. It also drives heat up into the crust at a much greater rate than Kelvin envisioned.

That’s not to say that radioactivity didn’t have its own part to play in showing that Kelvin was wrong. Physicists realized that the tick-tock of radioactive decay created a clock that they could use to estimate the age of rocks with exquisite precision. Thus we can now say that the Earth is not just billions of years old, but 4.567 billion.

Elegance unquestionably plays a big part in the advancement of science. The mathematical simplicity of quantum physics is lovely to behold. But in the hands of geologists, quantum physics has brought to light the glorious, messy, and very inelegant history of our planet.

[Post-script: Thanks to responses from readers, I can see how this essay is confusing. I added some passages from the papers I cite below down in the comment thread, which I hope can clear things up a bit.]

[Update: For an up-to-date review of the age and formation of the Earth, see this paper [abstract, free pdf] For a great look at Kelvin’s work, see this piece in American Scientist or the more technical paper on which it was based (free pdf).]

[Image: Photo by Hawaiian Sea - http://flic.kr/p/8AyKnC via Creative Commons]

Drew Berry is one of the great movie-makers of the molecular world. He makes gorgeous computer visualizations of DNA, proteins, and the various goings-on inside the cell. Last night I spent a little time watching a new TEDx talk of his just posted online. My first thought was, “Why didn’t I get to see these movies when I was learning about biology as a kid? Life is unfair.” Compared to the flat cartoons of textbooks, or even the crude animations in documentaries of yore, Berry’s work seems to come from some advanced alien civilization.

In case you haven’t seen Berry’s work before, I’ve embedded his lecture here. (You may have heard about him when he got a recent Macarthur “genius” grant.) If you have seen his stuff before, I’d suggest you watch this anyway. And this time, don’t just watch. Listen.

When I first saw Berry’s work a while back, I was immediately gob-smacked. But as I watched his synchronized swimming of molecules a while longer, I realized after a while that I didn’t understand a lot of what was going on. I didn’t know the names of the molecules I was looking at, and, more importantly, I couldn’t tell what a lot of them were doing. The only sense I could make of it all derived from what I already knew.

Berry’s TEDx talk is more satisfying because it’s a talk. You look at the mesmerizing images, and Berry explains what you’re seeing. What’s really interesting is how he–no doubt unconsciously–uses words that switch on the mental eye. When he zooms in on a chromosome, he points out structures passing through it that look “like whiskers,” which act as the “scaffolding” for the cell (the microtubules). He then zooms into the place where the chromosome and microtubule meet, the kinetochore. What you see looks like a supercomputer’s acid trip. But you can make sense of what you see because Berry uses metaphors. He calls it a “signal broadcasting system.” Now all the molecules jittering around aren’t totally random. We can see how molecules come together to make life possible.

There’s no question that people like Berry are going to be making the movies that fill our heads in our future when we think about what’s going on in our bodies. But those movies will need good soundtracks.

Cancer evolves. Those two words may sound strange together. Sure, birds evolve. Bacteria evolve. But cancer? The trouble arises from the fact that cancers, unlike birds and bacteria, are not free-living organisms. They start out as cells inside a person’s body and stay there, until they’re either wiped out or the person dies.*

Yet the same forces that drive the evolution of free-living organisms can also drive cancer cells to become more aggressive and dangerous. Evolution becomes our inner foe if mutations disable a cell’s self-restraint. The cell multiplies. Sometimes a new mutation arises in its descendants. If the mutations allow the cancer to grow faster, the cells carrying it will take over the population of cancerous cells. Natural selection and other processes that drive evolution on the outside start driving it on the inside.

Like so many other scientists, researchers who study cancer evolution have jumped on new technology for sequencing genomes on the cheap. They’re now starting to publish fine-grained histories of the disease, tracking individual mutations as they arise and spread. Nature has just published a fine example of this new research. I particularly appreciated the informative pictures they came up with to accompany the paper, one of which I’ve included here. You can click on the picture for a bigger version. And below the picture, I’ll explain what it means.

In the new paper, Li Ding and colleagues at Washington University describe a study they carried out on eight people suffering from acute myeloid leukemia (AML), a disease of the immune system. In people with AML, stem cells in the bone marrow that would normally turn into white blood cells instead become cancerous. Treatments include bone marrow transplants and chemotherapy. Unfortunately, AML has a nasty way of bouncing back from chemotherapy, and the drugs become useless to stop it. As a result, a lot of people who seem at first to be in remission eventually die of the cancer.

The Washington University scientists reconstructed the history of the cancer in each patients by sequencing genomes from a number of cells. To determine the normal, original genome, they sequenced DNA from a healthy skin cell. They then sequenced genomes from cancer cells taken from the patients when they were first diagnosed. And then they looked at genomes of cancer cells that emerged after the patients relapsed. From this survey, they came up with a catalog of new mutations that emerged over the course of the cancer. They could then go back into the blood samples and estimate what fraction of the cancer cells had a given mutation at a given point in time.

This figure illustrates the sad chronicle of one particular woman they studied. When she was in her late 50s, she suddenly came down with a sore throat and began to bruise easily. A bone marrow biopsy confirmed she has AML. She got chemotherapy, and then a stem cell transplant. Although she seemed to go into complete remission, the cancer returned 11 months after her diagnosis. The chemotherapy drugs that had previously been so effective now could not stop the cancer. Other drugs failed, too. Two years after her diagnosis, she died.

On the left of the figure, the cancer begins. A single stem cell mutated and became the founder of the cancerous lineage. we start with normal cells. (The cell is dark, and the grey dot marks its original mutation. HSC stands for hematopoietic stem cells).

The cancer cells grew in number, and as they did, they accumulated a lot of mutations, some of which are listed in the figure next to the star. All of these mutations, one after the other, took over the entire population of cells–a signature of natural selection. When the woman went to her doctor, however, the cancer had diversified into a number of different lineage, each carrying additional, distinctive mutations. Over half of the cells belonged to a lineage marked here in purple, known as cluster 2. Cluster 3, marked in yellow, was made up cells with a separate set mutations. And from within Cluster 3 emerged yet another lineage–Cluster 4, marked in orange. The dots in each circle show the sets of mutations that accumulated in each cluster.

The chemotherapy knocked down all the clusters of cancer cells to such low numbers that doctors couldn’t find them any more. But they were still there. And when exposed to chemotherapy drugs, the most successful cluster was not the one that had been most successful back when the cancer was diagnosed. It was the relatively rare Cluster 4. Apparently, it had mutations that made it better able to withstand the chemotherapy drugs. Some its descendants later picked up new mutations, which enabled them to reproduce quickly and take over the cancer population, as they resisted new chemotherapy drugs as well.

“The AML genome in an individual patient is clearly a ‘moving target,’” the scientists right conclude. “Eradication of the founding clone and all of its subclones will be required to achieve cures.” Easier said than done, of course. The parallels between this research and studies on antibiotic resistance in bacteria are sobering. But at least now we’re starting to see what kind of evolutionary challenge we’re really up against.

(*For one very cool exception to this rule, consider the case of Tasmanian devil facial tumors, which travel from devil to devil. They evolve too, though.)